Intrathecal-specific glutamic acid decarboxylase antibodies at low titers in autoimmune neurological disorders

Sunwoo, Jun Sang; Chu, Kon; Byun, Jung Ick; Moon, Jangsup; Lim, Joo Hyun; Kim, Tae Joon; Lee, Sang Kun; Jung, Kwangyun; Park, Kyung‐Il; Jeon, Daejong; Jung, Ki-Young; Kim, Manho

doi:10.1016/j.jneuroim.2015.11.012

Cited by 15 publications

(8 citation statements)

References 40 publications

(56 reference statements)

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“…Moreover, these patients had anti-GAD positivity in serum [4]. Recently, Sunwoo and colleagues described patients with anti-GAD antibodies in CSF but not in paired serum samples [5]. In this series, the most frequent clinical syndromes were limbic encephalitis and temporal lobe epilepsy, whereas cerebellar ataxia was less frequent and stiff person syndrome was very rare.…”

Section: Discussionmentioning

confidence: 73%

“…In this series, the most frequent clinical syndromes were limbic encephalitis and temporal lobe epilepsy, whereas cerebellar ataxia was less frequent and stiff person syndrome was very rare. None of these patients manifested extrapyramidal signs [5]. Polyclonality of anti-GAD antibody may theoretically explain such clinical variability [6], and clinical presentation and anti-GAD titers do not always correlate.…”

Section: Discussionmentioning

confidence: 95%

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Atypical parkinsonism and intrathecal anti-glutamic acid decarboxylase antibodies – an unusual association: a case report

et al. 2020

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Background: Immunological causes of parkinsonism are very rare and usually characterized by early presentation, poor response to levodopa, and additional clinical features. Case presentation: We describe a 58-year-old white man who presented with a 1-year history of gait disturbance with disequilibrium leading to falls. We report an association between parkinsonism and presence of anti-glutamic acid decarboxylase antibodies in his cerebrospinal fluid, discussing clinical presentation and follow-up. Conclusions: Besides the possibility of a casual association, this case allows us to hypothesize an alternative pathophysiological mechanism of parkinsonism implying interference with glutamic acid decarboxylase and gamma-aminobutyric acid functions, eventually resulting in basal ganglia circuit dysregulation.

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Section: Discussionmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 95%

Atypical parkinsonism and intrathecal anti-glutamic acid decarboxylase antibodies – an unusual association: a case report

et al. 2020

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“…Besides a well‐known association with Stiff‐person syndrome and ataxia and much rarer progressive encephalomyelitis with rigidity and myoclonus, few cases of movement disorders associated with anti‐GAD have been reported. Sunwoo and colleagues described 2 patients, 1 with oromandibular dyskinesia and limb dystonia and another with blepharospasm, jaw deviation, and face and neck dystonia, whereas Rachanna and Tarannum presented a case of parkinsonism and dysautonomia. Pittcock and colleagues reported a series of 62 positive anti‐GAD patients, including 10 with extrapyramidal features: axial or neck rigidity (8), parkinsonism (4), hyperkinetic dysarthria (1), posture‐sensitive dystonia (1), blepharospasm (1), and chorea (1).…”

Section: Discussionmentioning

confidence: 99%

Anti–Glutamic Acid Decarboxylase Encephalitis Presenting With Choreo‐Dystonic Movements and Coexisting Electrographic Seizures

Kauppila

Coelho

Franco

et al. 2019

Movement Disord Clin Pract

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“…Classic paraneoplastic autoantibodies, such as anti‐Hu, ‐Yo, ‐Ri, ‐CV2, ‐Ma2, ‐amphiphysin, ‐recoverin, ‐SOX1, and ‐titin were also screened using the immunoblotting method (Euroimmun). Anti‐glutamic acid decarboxylase (GAD) antibody levels were measured by radioimmunoassay (RSR Limited, Cardiff, UK), as previously described 15. Possible infectious etiologies were excluded according to a protocol previously described 5.…”

Section: Methodsmentioning

confidence: 99%

Bortezomib treatment for severe refractory anti‐NMDA receptor encephalitis

Shin

Lee

Kim

et al. 2018

Ann Clin Transl Neurol

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ObjectiveTo evaluate the therapeutic potential of bortezomib, a proteasome inhibitor that target plasma cells, in order to revive stalled recovery in patients with anti‐N‐methyl‐d‐aspartate (NMDA) receptor encephalitis who remain bedridden even after aggressive immunotherapy.MethodsWe consecutively enrolled patients with anti‐NMDA receptor encephalitis who remained bedridden after first‐line immunotherapy (steroids and intravenous immunoglobulin), second‐line immunotherapy (rituximab), and tocilizumab treatment, and treated them with subcutaneous bortezomib. Clinical response, functional recovery, and changes in antibody titer in the serum and cerebrospinal fluid were measured.ResultsBefore the bortezomib treatment, the five patients with severe refractory anti‐NMDA receptor encephalitis were in a vegetative state. During the 8 months of follow‐up period, three patients improved to minimally conscious states within 2 months of bortezomib treatment, one failed to improve from a vegetative state. However, no patient achieved functional recovery as measured by the modified Rankin Scale score (mRS). Three patients advanced to a cyclophosphamide with bortezomib and dexamethasone regimen, which only resulted in additional adverse events, without mRS improvement. Among the four patients whose antibody titer was followed, two demonstrated a twofold decrease in the antibody titer in serum and/or cerebrospinal fluid after 2 cycles of bortezomib.InterpretationAlthough there were some improvements in severe refractory patients, clinical response to bortezomib was limited and not clearly distinguishable from the natural course of the disease. The clinical benefit of bortezomib in recent studies requires further validation in different clinical settings.

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Intrathecal-specific glutamic acid decarboxylase antibodies at low titers in autoimmune neurological disorders

Cited by 15 publications

References 40 publications

Atypical parkinsonism and intrathecal anti-glutamic acid decarboxylase antibodies – an unusual association: a case report

Atypical parkinsonism and intrathecal anti-glutamic acid decarboxylase antibodies – an unusual association: a case report

Anti–Glutamic Acid Decarboxylase Encephalitis Presenting With Choreo‐Dystonic Movements and Coexisting Electrographic Seizures

Bortezomib treatment for severe refractory anti‐NMDA receptor encephalitis

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